ORIGINAL RESEARCH—WOMEN'S SEXUAL HEALTH: Successful Transcutaneous Electrical Nerve Stimulation in Two Women with Restless Genital Syndrome: The Role of Aδ- and C-Nerve Fibers

Abstract

Currently, efficacious treatment of restless genital syndrome (ReGS) is not available. This study aimed to report the results of transcutaneous electrical nerve stimulation (TENS) for ReGS, being a combination of genital dysesthesias, imminent and/or spontaneous orgasms, and/or restless legs, and/or overactive bladder. Two women with ReGS were referred to our clinic. In-depth interview, routine and hormonal investigations, electroencephalography, magnetic resonance imaging (MRI) of the brain and pelvis, manual examination of the ramus inferior of the pubic bone, and sensory testing of genital dermatomes were performed. Conventional TENS (frequency: 110 Hz; pulse width: 80 milliseconds) was applied bilaterally at the region of the pudendal dermatome in which immediate reduction of genital sensations occurred. Patients were instructed for self-application of TENS each day for 2 months. Oral report, questionnaires on frequency of imminent and/or spontaneous orgasms, combined with questions on intensity of restless genital feelings, restless leg syndrome (RLS), overactive bladder syndrome (OAB), and satisfaction with TENS treatment. ReGS in a 56-year-old woman manifested as multiple spontaneous orgasms, RLS, and OAB. TENS applied to the sacral region resulted in immediate reduction of complaints and a 90% reduction of spontaneous orgasms, RLS, and OAB in 2 months. ReGS in a 61-year-old woman manifested as a continuous restless genital feeling, imminent orgasms, and OAB. TENS applied to the pubic bone resulted in a complete disappearance of restlessness in the genital area as well as OAB complaints in 2 months. Both women reported to be very satisfied and did not want to stop TENS treatment. Conventional TENS treatment is a promising therapy for ReGS, but further controlled research is warranted. Preorgasmic and orgasmic genital sensations in ReGS are transmitted by Adelta and C fibers and are inhibited by Abeta fibers. A neurological hypothesis on the pathophysiology of ReGS encompassing its clinical symptomatology, TENS, and drug treatment is put forward.